The journal of pain : official journal of the American Pain Society
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Randomized Controlled Trial
Hypoalgesic effect of the transcutaneous electrical nerve stimulation following inguinal herniorrhaphy: a randomized, controlled trial.
We investigated the effect of transcutaneous electrical nerve stimulation (TENS) for inguinal herniorrhaphy postoperative pain control in a prospective, randomized, double-blinded, placebo-controlled study. Forty patients undergoing unilateral inguinal herniorrhaphy with an epidural anesthetic technique were randomly allocated to receive either active TENS or placebo TENS. Postoperative pain was evaluated using a standard 10-point numeric rating scale (NRS). Analgesic requirements were also recorded. TENS (100 Hz, strong but comfortable sensory intensity) was applied for 30 minutes through 4 electrodes placed around the incision twice, 2 and 4 hours after surgery. Pain was assessed before and after each application of TENS and 8 and 24 hours after surgery. In the group treated with active TENS, pain intensity was significantly lower 2 hours (P = .028), 4 hours (P = .022), 8 hours (P = .006), and 24 hours (P = .001) after the surgery when compared with the group that received placebo TENS. Active TENS also decreased analgesic requirements in the postoperative period when compared with placebo TENS (P = .001). TENS is thus beneficial for postoperative pain relief after inguinal herniorrhaphy; it has no observable side effects, and the pain-reducing effect continued for at least 24 hours. Consequently, the routine use of TENS after inguinal herniorrhaphy is recommended. ⋯ This study presents the hypoalgesic effect of high-frequency TENS for postoperative pain after inguinal herniorrhaphy. This may reinforce findings from basic science showing an opioid-like effect provided by TENS, given that high-frequency TENS has been shown to activate delta-opioid receptors.
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Chronic pain commonly accompanies long-term disabilities such as spinal cord injury (SCI). Research suggests that patient motivation to engage in adaptive pain coping strategies, such as exercise/stretching and task persistence, is an important factor in determining the impact that this pain will have on quality of life. One recently proposed model (the Motivational Model of Pain Self-Management) suggests that motivation to manage pain is influenced by 2 primary variables: Beliefs about the importance of engaging in pain self-management (ie, perceived importance) and beliefs about one's own ability to engage in these behaviors (ie, self-efficacy). The purpose of this study was to provide a preliminary test of this model in a sample of 130 adults with SCI who completed a return by mail survey. Measures included a numerical rating scale of pain intensity and the revised version of the Multidimensional Pain Readiness to Change Questionnaire. Mediation analyses were performed using multiple regression. Results suggested that the effects of perceived importance and self-efficacy on exercise behavior were mediated by readiness to engage in exercise, consistent with the proposed model. However, the model could not be established for the outcome of task persistence. ⋯ This study tests a model describing motivation to engage in pain management behaviors (ie, "readiness to change") in adults with SCI. This model could potentially aid clinicians in their conceptualization of the factors that affect patient motivation to manage pain.
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Symptoms of post-traumatic stress disorder (PTSD) are a common comorbidity in patients with a history of accident-related chronic pain and depression. However, little is known regarding the influence of PTSD in contributing to the affective distress, pain experience, and disability associated with chronic pain in this population. This study used structural equation modeling to examine 3 models that assess these relations in a sample of chronic pain patients with accident-related pain. Subjects were assessed for pain experience, depressive symptoms, anxiety, PTSD symptoms, pain disability, and relevant demographic variables. Pearson correlations indicated that symptoms of depression were significantly related to more severe pain, disability, and PTSD symptoms. PTSD symptoms were significantly associated with higher disability. The model of best fit indicated that after controlling for the influence of anxiety on the dependent measures, PTSD symptoms have a direct influence on severity of depressive symptoms, whereas depressive symptoms have a direct influence on pain intensity and an indirect impact on pain intensity by way of their effect on disability. These data point to the importance of unresolved PTSD symptoms in contributing to the level of depression, pain, and disability exhibited by chronic pain patients and highlight the need to consider directed and primary treatment of PTSD in pain rehabilitation programs. ⋯ This study highlights the impact of symptoms of PTSD on levels of depression, disability, and pain in patients with pain secondary to physical injury. Our results suggest that pain rehabilitation programs provide directed interventions for PTSD symptoms among this population to improve pain treatment outcomes.
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Chronic pain conditions remain a high unmet medical need, and a significant number of patients are not effectively treated with currently available therapies. There is a significant challenge in developing more effective therapies to treat pain, particularly in chronic debilitating pain conditions such as neuropathic pain. Preclinical research has been beneficial in advancing mechanistic understanding of the pathophysiology of pain as well as in defining new therapeutic targets for intervention. However, the increased understanding of the neurobiology of pain has not yet translated into breakthroughs in pain therapies. Some debate exists as to how predictive the common animal models of pain are to the human condition. Translation animal model activity promises to be enhanced by application of novel neuroimaging technologies. It is well acknowledged throughout the industry that the application of preclinical to clinical translational biomarkers is an important strategy that holds promise in increasing the confidence in the translatability of the preclinical to clinical data. Imaging biomarkers have tremendous potential for affecting pain research from both diagnostic as well as therapeutic standpoints. Noninvasive imaging has the inherent advantage of being able to evaluate central mechanisms of pain and the effects of intervention both in animals and in humans. Because each subject serves as its own control, the inherent intersubject variabilities can be less of a confound. This review discusses both the promise and limitations of using imaging modalities to study pain processing and integrates it into the evolving drug discovery and development paradigm. Each section summarizes current clinical reports and, if applicable, preclinical translational findings. Emphasis is given to technical areas for future development and revealing neuroinflammation dynamics and targets that are influenced by genetics and cellular insults. With continued application of neuroimaging technologies, new therapeutic approaches to treat chronic pain as well as define tools to assess functional outcomes promise to emerge. ⋯ This review discusses the promises and limitations of using noninvasive imaging modalities to study pain processing and integrates it into the evolving drug discovery and development paradigm. Emerging neuroimaging technologies may spawn new therapeutic approaches to treat chronic pain as well as define translational tools to assess functional clinical outcomes.
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The objectives of this study were to test the feasibility of measuring inflammatory and nociceptive biochemical mediators at the surgical site and to evaluate the relationship between wound and serum levels as well as determine any associations between mediator release, pain, and analgesic consumption after cesarean delivery. Twenty healthy women undergoing elective cesarean delivery with spinal anesthesia were enrolled. Wound exudate and serum mediators, pain scores, and analgesic consumption were measured at 1, 6, 24, and 48 hours after cesarean. In wound exudate, 19 of 20 mediators were reliably detected including interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17, tumor necrosis factor-alpha, interferon-gamma, granulocyte colony stimulating factor (G-CSF), granulocyte-macrophage colony stimulating factor (GM-CSF), monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein 1 (MIP-1beta), nerve growth factor (NGF), prostaglandin E2 (PG-E2), and substance P. Wound PG-E2 and various cytokines peaked early, whereas NGF showed a more delayed release. There were no correlations between the concentration versus time profile of wound and serum cytokines. Analgesic consumption during the first 24 hours after surgery was negatively correlated with IL-1beta, IL-6, and G-CSF in the wound exudate. This study demonstrates the feasibility of collecting and measuring nociceptive and inflammatory mediators in surgical wounds at specific time points. The lack of significant correlations between wound and serum levels emphasizes the importance of determining site-specific release if localized pathologies are to be studied. ⋯ This study demonstrates the feasibility of measuring real-time nociceptive and inflammatory mediators in surgical wounds. Our findings confirm the lack of correlation between wound and serum levels of many pro-inflammatory and anti-inflammatory cytokines and nerve growth factor.